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Cancers
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Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and...
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Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 16586

Special Issue Editors

Prof. Dr. Marikki Laiho

E-Mail Website
Guest Editor
Division of Molecular Radiation Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA
Interests: DNA damage biology; regulation and targeting of RNA polymerase I transcription; nucleolar stress response
Dr. Michael Goldstein

E-Mail Website
Guest Editor
Department of Radiation Oncology and Molecular Radiation Sciences, Johns Hopkins School of Medicine, Baltimore, MD, USA
Interests: DNA damage responses; epigenetics; radiation oncology

Special Issue Information

Dear Colleagues,

The area of DNA damage response (DDR) has been expanding over the past decades providing important insights into cellular mechanisms of DNA damage recognition, signalling and repair.

Radiotherapy is a cornerstone for treatment of various types of cancer. Since radiation kills tumor cells by damaging their DNA understanding the molecular mechanisms of DDR in tumor cells opens new avenues for improvement of radiotherapy.

In this regard, an alteration in DNA damage signaling can result in radiation resistance and tumor progression. In contrast, a dependence of cancer cells on specific DDR pathways can be targeted to improve the efficacy of radiation. Notably, multiple epigenetic signaling pathways facilitating DDR have been identified providing an additional layer of DDR regulation that can be exploited for sensitizing cancer to radiation. Finally, complex DNA damage induced by new radiotherapy modalities such as particle radiation requires an intricate orchestration of multiple DDR pathways allowing for an improved therapeutic window in tumors with certain DNA repair defects.

All of these aspects of radiation-induced DNA damage and response mechanisms will be addressed in our Special Issue providing perspectives for the future development of radiotherapy.

We are pleased to invite you to contribute a Research Paper or a Review focusing on radiation-induced DNA damage and DNA damage response in cancer. We are particularly interested in contributions that emphasize cancer-specific signalling pathways that can be exploited for therapeutic purposes including epigenetic signaling pathways as well as a combination of radiotherapy with molecular therapeutics targeting DDR. Additionally, we welcome contributions focusing on tumor response to complex DNA damage induced by particle therapy.

This Special Issue aims to illustrate the significance of DNA damage signaling in tumor response to radiation and provide perspectives on targeting these pathways to enhance the efficacy of radiotherapy.

We look forward to receiving your contributions.

Prof. Dr. Marikki Laiho
Dr. Michael Goldstein
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • DNA damage
  • DNA damage response
  • radiation
  • DNA repair
  • epigenetics
  • chromatin modification
  • complex DNA damage

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Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 5196 KiB  
Article
Amino Terminal Acetylation of HOXB13 Regulates the DNA Damage Response in Prostate Cancer
by Duy T. Nguyen, Urvashi Mahajan, Duminduni Hewa Angappulige, Aashna Doshi, Nupam P. Mahajan and Kiran Mahajan
Cancers 2024, 16(9), 1622; https://doi.org/10.3390/cancers16091622 - 23 Apr 2024
Viewed by 2247
Abstract
Advanced localized prostate cancers (PC) recur despite chemotherapy, radiotherapy and/or androgen deprivation therapy. We recently reported HOXB13 lysine (K)13 acetylation as a gain-of-function modification that regulates interaction with the SWI/SNF chromatin remodeling complex and is critical for anti-androgen resistance. However, whether acetylated HOXB13 [...] Read more.
Advanced localized prostate cancers (PC) recur despite chemotherapy, radiotherapy and/or androgen deprivation therapy. We recently reported HOXB13 lysine (K)13 acetylation as a gain-of-function modification that regulates interaction with the SWI/SNF chromatin remodeling complex and is critical for anti-androgen resistance. However, whether acetylated HOXB13 promotes PC cell survival following treatment with genotoxic agents is not known. Herein, we show that K13-acetylated HOXB13 is induced rapidly in PC cells in response to DNA damage induced by irradiation (IR). It colocalizes with the histone variant γH2AX at sites of double strand breaks (DSBs). Treatment of PCs with the Androgen Receptor (AR) antagonist Enzalutamide (ENZ) did not suppress DNA-damage-induced HOXB13 acetylation. In contrast, HOXB13 depletion or loss of acetylation overcame resistance of PC cells to ENZ and synergized with IR. HOXB13K13A mutants show diminished replication fork progression, impaired G2/M arrest with significant cell death following DNA damage. Mechanistically, we found that amino terminus regulates HOXB13 nuclear puncta formation that is essential for proper DNA damage response. Therefore, targeting HOXB13 acetylation with CBP/p300 inhibitors in combination with DNA damaging therapy may be an effective strategy to overcome anti-androgen resistance of PCs. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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15 pages, 5116 KiB  
Article
Investigating the Use of a Liquid Immunogenic Fiducial Eluter Biomaterial in Cervical Cancer Treatment
by Michele Moreau, Lensa S. Keno, Debarghya China, Serena Mao, Shahinur Acter, Gnagna Sy, Hamed Hooshangnejad, Kwok Fan Chow, Erno Sajo, Jacques Walker, Philmo Oh, Eric Broyles, Kai Ding, Akila Viswanathan and Wilfred Ngwa
Cancers 2024, 16(6), 1212; https://doi.org/10.3390/cancers16061212 - 20 Mar 2024
Cited by 2 | Viewed by 2095
Abstract
Globally, cervical cancer is the fourth leading cancer among women and is dominant in resource-poor settings in its occurrence and mortality. This study focuses on developing liquid immunogenic fiducial eluter (LIFE) Biomaterial with components that include biodegradable polymers, nanoparticles, and an immunoadjuvant. LIFE [...] Read more.
Globally, cervical cancer is the fourth leading cancer among women and is dominant in resource-poor settings in its occurrence and mortality. This study focuses on developing liquid immunogenic fiducial eluter (LIFE) Biomaterial with components that include biodegradable polymers, nanoparticles, and an immunoadjuvant. LIFE Biomaterial is designed to provide image guidance during radiotherapy similar to clinically used liquid fiducials while enhancing therapeutic efficacy for advanced cervical cancer. C57BL6 mice were used to grow subcutaneous tumors on bilateral flanks. The tumor on one flank was then treated using LIFE Biomaterial prepared with the immunoadjuvant anti-CD40, with/without radiotherapy at 6 Gy. Computed tomography (CT) and magnetic resonance (MR) imaging visibility were also evaluated in human cadavers. A pharmacodynamics study was also conducted to assess the safety of LIFE Biomaterial in healthy C57BL6 female mice. Results showed that LIFE Biomaterial could provide both CT and MR imaging contrast over time. Inhibition in tumor growth and prolonged significant survival (* p < 0.05) were consistently observed for groups treated with the combination of radiotherapy and LIFE Biomaterial, highlighting the potential for this strategy. Minimal toxicity was observed for healthy mice treated with LIFE Biomaterial with/without anti-CD40 in comparison to non-treated cohorts. The results demonstrate promise for the further development and clinical translation of this approach to enhance the survival and quality of life of patients with advanced cervical cancer. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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Review

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14 pages, 560 KiB  
Review
Mechanisms Underlying the Development of Murine T-Cell Lymphoblastic Lymphoma/Leukemia Induced by Total-Body Irradiation
by Toshihiko Sado, John B. Cart and Chang-Lung Lee
Cancers 2024, 16(12), 2224; https://doi.org/10.3390/cancers16122224 - 14 Jun 2024
Viewed by 1440
Abstract
Exposure to ionizing radiation is associated with an increased risk of hematologic malignancies in myeloid and lymphoid lineages in humans and experimental mice. Given that substantial evidence links radiation exposure with the risk of hematologic malignancies, it is imperative to deeply understand the [...] Read more.
Exposure to ionizing radiation is associated with an increased risk of hematologic malignancies in myeloid and lymphoid lineages in humans and experimental mice. Given that substantial evidence links radiation exposure with the risk of hematologic malignancies, it is imperative to deeply understand the mechanisms underlying cellular and molecular changes during the latency period between radiation exposure and the emergence of fully transformed malignant cells. One experimental model widely used in the field of radiation and cancer biology to study hematologic malignancies induced by radiation exposure is mouse models of radiation-induced thymic lymphoma. Murine radiation-induced thymic lymphoma is primarily driven by aberrant activation of Notch signaling, which occurs frequently in human precursor T-cell lymphoblastic lymphoma (T-LBL) and T-cell lymphoblastic leukemia (T-ALL). Here, we summarize the literature elucidating cell-autonomous and non-cell-autonomous mechanisms underlying cancer initiation, progression, and malignant transformation in the thymus following total-body irradiation (TBI) in mice. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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17 pages, 1353 KiB  
Review
The Causes and Consequences of DNA Damage and Chromosomal Instability Induced by Human Papillomavirus
by Kathryn M. Jones, Ava Bryan, Emily McCunn, Pate E. Lantz, Hunter Blalock, Isabel C. Ojeda, Kavi Mehta and Pippa F. Cosper
Cancers 2024, 16(9), 1662; https://doi.org/10.3390/cancers16091662 - 25 Apr 2024
Cited by 5 | Viewed by 2318
Abstract
High-risk human papillomaviruses (HPVs) are the main cause of cervical, oropharyngeal, and anogenital cancers, which are all treated with definitive chemoradiation therapy when locally advanced. HPV proteins are known to exploit the host DNA damage response to enable viral replication and the epithelial [...] Read more.
High-risk human papillomaviruses (HPVs) are the main cause of cervical, oropharyngeal, and anogenital cancers, which are all treated with definitive chemoradiation therapy when locally advanced. HPV proteins are known to exploit the host DNA damage response to enable viral replication and the epithelial differentiation protocol. This has far-reaching consequences for the host genome, as the DNA damage response is critical for the maintenance of genomic stability. HPV+ cells therefore have increased DNA damage, leading to widespread genomic instability, a hallmark of cancer, which can contribute to tumorigenesis. Following transformation, high-risk HPV oncoproteins induce chromosomal instability, or chromosome missegregation during mitosis, which is associated with a further increase in DNA damage, particularly due to micronuclei and double-strand break formation. Thus, HPV induces significant DNA damage and activation of the DNA damage response in multiple contexts, which likely affects radiation sensitivity and efficacy. Here, we review how HPV activates the DNA damage response, how it induces chromosome missegregation and micronuclei formation, and discuss how these factors may affect radiation response. Understanding how HPV affects the DNA damage response in the context of radiation therapy may help determine potential mechanisms to improve therapeutic response. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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34 pages, 2995 KiB  
Review
Exploiting the DNA Damage Response for Prostate Cancer Therapy
by Travis H. Stracker, Oloruntoba I. Osagie, Freddy E. Escorcia and Deborah E. Citrin
Cancers 2024, 16(1), 83; https://doi.org/10.3390/cancers16010083 - 23 Dec 2023
Cited by 5 | Viewed by 2822
Abstract
Prostate cancers that progress despite androgen deprivation develop into castration-resistant prostate cancer, a fatal disease with few treatment options. In this review, we discuss the current understanding of prostate cancer subtypes and alterations in the DNA damage response (DDR) that can predispose to [...] Read more.
Prostate cancers that progress despite androgen deprivation develop into castration-resistant prostate cancer, a fatal disease with few treatment options. In this review, we discuss the current understanding of prostate cancer subtypes and alterations in the DNA damage response (DDR) that can predispose to the development of prostate cancer and affect its progression. We identify barriers to conventional treatments, such as radiotherapy, and discuss the development of new therapies, many of which target the DDR or take advantage of recurring genetic alterations in the DDR. We place this in the context of advances in understanding the genetic variation and immune landscape of CRPC that could help guide their use in future treatment strategies. Finally, we discuss several new and emerging agents that may advance the treatment of lethal disease, highlighting selected clinical trials. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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28 pages, 2218 KiB  
Review
Novel Mechanisms and Future Opportunities for the Management of Radiation Necrosis in Patients Treated for Brain Metastases in the Era of Immunotherapy
by Eugene J. Vaios, Sebastian F. Winter, Helen A. Shih, Jorg Dietrich, Katherine B. Peters, Scott R. Floyd, John P. Kirkpatrick and Zachary J. Reitman
Cancers 2023, 15(9), 2432; https://doi.org/10.3390/cancers15092432 - 24 Apr 2023
Cited by 12 | Viewed by 4547
Abstract
Radiation necrosis, also known as treatment-induced necrosis, has emerged as an important adverse effect following stereotactic radiotherapy (SRS) for brain metastases. The improved survival of patients with brain metastases and increased use of combined systemic therapy and SRS have contributed to a growing [...] Read more.
Radiation necrosis, also known as treatment-induced necrosis, has emerged as an important adverse effect following stereotactic radiotherapy (SRS) for brain metastases. The improved survival of patients with brain metastases and increased use of combined systemic therapy and SRS have contributed to a growing incidence of necrosis. The cyclic GMP-AMP (cGAMP) synthase (cGAS) and stimulator of interferon genes (STING) pathway (cGAS-STING) represents a key biological mechanism linking radiation-induced DNA damage to pro-inflammatory effects and innate immunity. By recognizing cytosolic double-stranded DNA, cGAS induces a signaling cascade that results in the upregulation of type 1 interferons and dendritic cell activation. This pathway could play a key role in the pathogenesis of necrosis and provides attractive targets for therapeutic development. Immunotherapy and other novel systemic agents may potentiate activation of cGAS-STING signaling following radiotherapy and increase necrosis risk. Advancements in dosimetric strategies, novel imaging modalities, artificial intelligence, and circulating biomarkers could improve the management of necrosis. This review provides new insights into the pathophysiology of necrosis and synthesizes our current understanding regarding the diagnosis, risk factors, and management options of necrosis while highlighting novel avenues for discovery. Full article
(This article belongs to the Special Issue Recent Perspectives on Mechanisms of Radiation-Mediated DNA Damage Induction and Response in Cancers)
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